Quotes from Doctors & Researchers:

It is often claimed that scientists and doctors are united in their belief in the value of, and necessity for, animal experiments to protect human health. This stream of quotes from scientists and doctors, stretching from as far back as the early 20th Century right up to today, shows that there has been a long tradition of scepticism about this issue. Many of the quotes are from scientists who support or conduct animal research; far from diminishing the impact of their words, this fact ought to give them extra weight.

Note: FDA stands for Food and Drug Administration, the US drug regulatory body.

Cancer

2013

"I'm a cancer researcher, and the traditional model for testing drugs which are used for cancer therapy is to use a mouse. But recently, there have been great advances made in the laboratory in growing cancer cells in dishes, and I think it's got to the stage where, in many situations, this provides a much more accurate model than the mouse. Appropriate development of new laboratory tests which are effective and meaningful could reduce the number of animals used by half. It would have advantages for the mice - but it would also have a lot of advantages for people - because this could actually increase the rate at which we develop drugs, and that would be in itself very valuable."
Professor Ian Mackenzie, Professor of Stem Cell Science, Blizard Institute, London, BBC Radio 4 Today Programme, 31 July 2013: http://www.bbc.co.uk/programmes/b037j0h8/live

2011

Indeed, because oncology drugs have a success rate of only 5%, it is clear that animal models are only marginally effective.
M.B. Esch, T.L. King and M.L. Shuler, The Role of Body-on-a-Chip Devices in Drug and Toxicity Studies, Annu. Rev. Biomed. Eng. 2011. 13:55–72 (doi:10.1146/annurev-bioeng-071910-124629)2010

Mouse models that use transplants of human cancer have not had a great track record of predicting human responses to treatment in the clinic. It’s been estimated that cancer drugs that enter clinical testing have a 95 percent rate of failing to make it to market, in comparison to the 89 percent failure rate for all therapies . . . Indeed, “we had loads of models that were not predictive, that were [in fact] seriously misleading,” says NCI’s Marks, also head of the Mouse Models of Human Cancers Consortium. The Scientist, April 1, 2010

2008

Mouse xenograft models of cancer, understandably, have a
terrible reputation. Although researchers and companies routinely use these
human tumors in mice for preclinical drug testing, individual models poorly
predict how drugs will act in the clinic. Retrospective reviews published by
the National Cancer Institute in 2001 and the National Cancer Institute of
Canada in 2003 came to the same conclusion: Drugs that work againstcancer in
xenograft mice rarely work in people with the same tumor, with the exception of
lung and possibly ovarian cancer. "There's this mantra: 'Xenografts don't
predict for human effects,'" said Peter Houghton, Ph.D., a cancer
researcher at the St. Jude Children's Research Hospital in Memphis, Tennessee. Ken Garber, Journal of the National Cancer
Institute, 30th December.

"Animals don't reflect the reality of cancer in humans," says Fran Visco, who was diagnosed with breast cancer in 1987 and four years later founded the National Breast Cancer Coalition, an advocacy group. "We cure cancer in animals all the time, but not in people." Even scientists who have used animal models to make signal contributions to cancer treatment agree. "Far more than anything else," says Robert Weinberg of MIT, the lack of good animal models "has become the rate-limiting step in cancer research" - Sharon Begley, Newsweek, September 6th

"Animal models have not been very predictive of how well drugs would do in people," says oncologist Paul Bunn, who leads the International Society for the Study of Lung Cancer. "We put a human tumor under the mouse's skin, and that microenvironment doesn't reflect a person's—the blood vessels, inflammatory cells or cells of the immune system," all of which affect prognosis and survival - Sharon Begley, Newsweek, September 6th

2007

We have
learned well how to treat cancer in mice and rats but we still can’t cure
people. Professor Colin Garner, quoted in
Accelerator MS Is a Powerful New Tool, Genetic Engineering &
Biotechnology News, Vol. 27, No. 15.

2006

We do trials in people because animal models do not predict what
will happen in humans. Dr
Sally Burtles, Cancer Research UK, Report of the Expert Scientific Group on
phase one clinical trials, following the TGN1412 clinical trial disaster.

You really
have to design the medicine for the species of interest…You'll find it very
rare to find a medicine that will work in both…Patrick M. O'Connor, head of oncology research for
Pfizer, quoted in The New York Times, 24 November.

In summary,
mouse xenograft models should not be viewed as ideal models for cancer drug
development. Altered, nonhuman host stroma, poor predictive value when applied
in an empirical sense, and questionable relation to the naturally occurring
human disease are but a few features, which temper enthusiasm for their use. Sausville & Burger, Cancer Research, 66, 3351-3354, April 1.

Even when
drugs with evidence of anticancer activity in preclinical in vivo models are
given at their maximum tolerated doses, they frequently fail to produce useful
activity in humans. Sausville & Burger, Cancer
Research, 66, 3351-3354, April 1.

In the U.S.
NCI retrospective(2001), activity in at least 33% of models of a variety of
histologiespredicted for clinical activity in some disease. In the
NCIof Canada retrospective (2003), generally similar conclusionswere reached.
It should be cautioned, however, that the drugsused in these
studies were for the most part "classic" cytotoxics.Whether
"targeted" therapeutics, such as signal transductioninhibitors,
antiangiogenic, or stroma-modifying agents, wouldperform better or
worse remains to be defined. Sausville &
Burger, Cancer Research, 66,
3351-3354, April 1.

Change is needed. Thirty years of experience with
subcutaneous xenografts, human tumors implanted under the skin of the mouse,
have satisfied few because so many drugs that cure cancer in these mice fail to
help humans. A 2004 analysis in the Journal of theAmerican Medical Association showed that only 3.8% of patients in phase I cancer
drug trials between 1991 and 2002 achieved an objective clinical response
— and the response rate is declining. Almost all drugs tried in humans work
against subcutaneous xenografts in mice. “How many more negative data do you
want? It’s very depressing.” said Isaiah Fidler , Ph.D., of the University of
Texas M. D. Anderson Cancer Research Center in Houston. Ken Garber, Journal of the National Cancer Institute,
Vol. 98, No. 17, September 6.

2005

Given that many of these investigational anticancer drugs eventually
fail, the animal models on which clinical trials are predicated must at best be
limited in power, and at worst wildly inaccurate. Dr Alexander Kamb, Global Head of the Oncology Disease
Area at the Novartis Institutes for Biomedical Research, Nature Reviews Drug
Discovery, 4, 161 - 165.

The problem
with animal carcinogenicity tests is not their lack of sensitivity for human
carcinogens, but rather their lack of human specificity. A positive result has
poor predictive value for humans. Knight, Bailey
& Balcombe, British Medical Journal USA, Vol. 5, p477.

2004

It’s been well known for maybe two decades that many of these
preclinical human cancer models have very little predictive power in terms of
how actual human beings – actual human tumours inside patients –
will respond…Preclinical models of human cancer, in large part, stink…Hundreds
of millions of dollars are being wasted every year by drug companies using
these [animal] models…Prof.
Robert Weinberg, Massachusetts Institute of Technology, Fortune, 9th March.

[mouse models are] woefully inadequate…if you look at
the millions and millions and millions of mice that have been cured, and you
compare that to the relative success, or lack thereof, that we've achieved in
the treatment of metastatic disease clinically, you realize that there just has
to be something wrong with those models. Homer Pearce, research fellow at Eli
Lilly. Fortune, 9th March.

2003

In Tamoxifen’s
case, a drug first developed as a potential contraceptive languished for many
years before its present application was found. Furthermore, its propensity to
cause liver tumours in rats, a toxicity problem that thankfully does not carry
over into humans, was not detected until after the drug had been on the market
for many years. If it had been found in preclinical testing, the drug would
almost certainly have been withdrawn from the pipeline.Nature Reviews Drug Discovery 2003; 2:167.

The in vitro cell
line model was predictive for non-smallcell lung cancer under the
disease-oriented approach, for breastand ovarian cancers under the
compound-oriented approach, andfor all four tumor types together.
The mouse allograft modelwas not predictive. The human xenograft
model was not predictivefor breast or colon cancers, but was
predictive for non-smallcell lung and ovarian cancers when panels
of xenografts wereused. Voskoglou et al. Clinical Cancer Research Vol. 9,
4227-4239.

2001

…some findings
in colon cancer mice, which were very good models, actually led to clinical
trials in humans which resulted in an increase in cancer. Dr Jeffrey E. Green of the National Cancer Institute’s
Laboratory of Cell Regulation and Carcinogenesis. Journal of the National
Cancer Institute, 93:976.

For 39 agents
with both xenograft data and Phase II clinical trials results available, in
vivo activity in a particular histology in a tumour model did not closely
correlate with activity in the same human cancer histology, casting doubt on
the correspondence of the pre-clinical models to clinical results. Johnson and colleagues, British Journal of Cancer, 84(10):1289-90.

1999

People are
very complacent with their animal models. But this begs the question of whether
there exists a good model of cancer. Dr Andy
Maniotis, The American Journal of Pathology, 155: 739.

1998

My own medical
perspective is that animal cancer research should be regarded as the scientific
equivalent of gossip – with about the same chance of turning out to be
true, i.e. truly effective in humans. Some gossip turns out to be true, but
most of it does not…and gossip can cause great anguish for those affected, in
this case millions of desperate cancer patients worldwide. G. Timothy Johnson MD, Boston Globe, May 22.

The history of
cancer research has been a history of curing cancer in the mouse. We have cured
mice of cancer for decades, and it simply didn’t work in humans. Dr Richard Klausner, Director,
National Cancer Institute, LA Times, May 6.

The
fundamental problem in drug discovery for cancer is that the model systems are
not predictive at all," says Alan Oliff, executive director for cancer
research at Merck Research Laboratories in West Point, Pennsylvania…Researchers
blamed the failures on the fact that the drugs were being tested against mouse,
not human, tumors… the xenograft tumors don't behave like naturally occurring
tumors in humans – they don't spread to other tissues, for example. Thus,
drugs tested in the xenografts appeared effective but worked poorly in humans.
"We had basically discovered compounds that were good mouse drugs rather
than good human drugs," says Sausville (associate director of the division
of cancer treatment and diagnosis, NCI). Science, 278; 1041-1042.

One might
expect that these animals would mimic human symptoms, not just the genetic
mutations. In fact, that is usually the exception, not the rule. Dr Tyler Jacks, regarding genetically modified mice in
cancer research. Science, 287:
1041.

1995

Since its
inception 25 years ago, EPA [the US Environmental Protection Agency] has
applied the same logic to hundreds of other substances, extrapolating from high
levels in animal studies to arrive at acceptable levels for humans. But that
approach, say scientists both inside and outside the federal government, may no
longer be the best way to safeguard public health...EPA's new emphasis on
molecular data is based on a growing body of evidence that extrapolations from
megadoses can provide a misleading picture of the effects of low-level exposure.
Chloroform is a good example. EPA's current strict standards were derived from
a study in which mice developed liver tumors after exposure to massive daily
doses of chloroform pumped into their stomachs over several months. However,
those findings may not be relevant to human exposures, according to a paper
picked by the Society of Toxicology as the best published last year in its
journal. Richard Stone, Science, vol 268, p 356-357.

1993

1-3 Butadiene,
an important industrial chemical and a common environmental air pollutant, has
been shown to be a weak carcinogen in the rat, but a potent carcinogen in the
B6C3F1 mouse. This species difference makes risk extrapolation to humans
difficult, and the underlying mechanism must be clarified before meaningful
risk extrapolation to humans can be made. Dr
Gunnar Johanson, of the National Institute of Occupational health, Sweden, Alternatives
to Laboratory Animals, vol 21, p
173180.

Why the dog
was ever considered as an appropriate animal for carcinogenicity testing is
also not entirely clear... Despite the obvious problems of study design and
interpretation, carcinogenicity tests in the dog, lasting 7 years, were
requested by regulatory authorities from the late 1960s...One of the best known
examples of the inappropriate use of the dog was the carcinogenicity testing of
hormonal contraceptives. It is now understood that mammogenesis in the dog is
very different from that in primates; quantitative and qualitative differences
exist in the feedback control mechanisms, receptor content and behaviour, and
target sensitivity and responsivity. As a result of this biological difference
there was a high incidence of mammary tumours in long-term studies in dogs
treated with progestagens/contraceptive steroids such as lynestrol. Ultimately
pressure from the scientific community led, relatively recently, to the
requirement for carcinogenicity studies in dogs being dropped. Parkinson and Grasso, Human and Experimental
Toxicology, vol 12, p 99-109.

1992

In the course
of tumour progression, it has been known for many years that mice and men are
totally different. Nature, Nov 26.

The following
quotes are all from Philip H Abelson, Science, vol 255, p 141.

- It has been conventional practice to test potential carcinogens
using highly inbred strains of rodents. The rationale was the supposed superior
reproducibility of results compared with those obtained from wild-type animals.
However, that assumption can be questioned. At least three examples of genetic
drift of inbred strains can be cited... Lifetime expectation [in an inbred
strain of mice] of developing one or another form of neoplasm ['spontaneous
tumour'] had risen from 10 to 80 percent.

- The
use of inbred strains as test animals can be further questioned on the basis
that they often develop spontaneous tumors in organs where cancers are not
frequent in humans. For example, incidences of mouse liver tumors in 2-yearold
B6C3F1 mice has ranged from 17.8 to 46.9 percent. In contrast, the death rate
from liver cancer in the United States is about 0.005 percent.

- Results
of the animal studies raise questions about the validity of federal regulations
that are based on ad lib-fed inbred strains of rodents. Are humans to be
regarded as behaving biochemically like huge, obese, inbred cancer-prone
rodents?

- The estimate made by NIOSH was 597 excess cancers per 10,000
workers having that same exposure... Instead of extra cancers predicted by
NIOSH, workers had fewer cancers than expected...With trillions of dollars,
loss of competitiveness, and jobs at stake, a searching review of the risk
assessment methodology of the regulatory agencies is overdue.

[Regarding
tamoxifen, an anti-cancer drug] "Experimentally, tamoxifen has
carcinogenic potential. In some strains of rat, but not mouse or hamster,
tamoxifen can cause liver cancers at doses as low as 5mg/kg per day... However,
there are doubts about the correlation of [the results] with the risk of
malignant disease even in rats, let alone in other rodents, mammals, or human
beings. There are many uncertainties in extrapolating these experimental data
from rats to women. The effect depends on bioavailability, hepatic [liver]
blood flow, and hepatic [liver] metabolism to active genotoxic carcinogens, all
of which differ enormously between rat and man. Dr
Trevor Powles, The Lancet, vol
340, p 1145-1147.

1991

For example,
the control incidence of mouse liver tumour varies between 0 and 58% in 41 NTP
[National Toxicology Program] bioassays where these tumours are induced by a
test chemical. Ashby and Morrod, Nature, vol 352, p 185-186.

Yes, I think
it is very clear to all of us who are engaged in the business of assessing
toxicity data that, when volumes of data are proudly presented to us after a
carcinogenicity study, showing that there was a tumour in this organ or that,
we look at it and we scratch our heads, and we wonder what on earth we can make
of it. This is especially true when huge doses are given, with nothing to
suggest what would be expected at low doses. I think very often the carcinogenicity
studies are a waste of everybody's time and a fearful waste of animals. They
are conducted partly because we are not sure what to do instead, and partly
because they are a political gesture and a very miserable one at that. Professor Andre McLean, speaking at a conference
reported in Animals and Alternatives in Toxicology, p86, ed. Balls, Bridges and Southee (publ.
Macmillan).

The
[pharmaceutical] industry is left with an expensive and time consuming test
which uses large numbers of animals and whose very basis is questioned by
scientists. Professor D Davies, quoted in the
pharmaceutical magazine Scrip, 2nd
October, p 23.

[Animal
carcinogenicity tests on new drugs are] inaccurate, often insensitive and
generally misleading. Dr John Griffin, Director
of the Association of British Pharmaceutical Industry, quoted in the
pharmaceutical magazine Scrip, 2nd
October, p 23.

It seems
sometimes that almost everything we eat, drink or take can cause cancer in
rats. That does not necessarily relate to tumours in humans. Tony Watson, President of the British Association of
Plastic Surgeons, quoted in The Times,
9th May.

1990

Our risk
models are based on at least 50 assumptions, none of which has been
scientifically demonstrated. For example, we assume that there is no difference
between continuous (as in animal tests) or intermittent (as in human
experience) dosages. But that ignores our growing knowledge of the way in which
DNA repairs the human system . . .We feed rodents `all-you-can-eat' buffets
every day, yet we know that caloric intake is the single greatest contributing
cause of cancer [in rodents]. In fact, we found you can modify the cancer
causing impact of one of the most potent carcinogens from 90% down to less than
3%, just by cutting caloric intake 20%. Dr.
Ronald Hart, Director of the Center for Toxicological Research in Arkansas,
quoted in Business Review Weekly,
27th April.

… Predictions
of carcinogenicity from laboratory animals are without meaning for there is no
evidence that the studies were conducted in a way that took into consideration
the pharmacodynamics in the species investigated, or with any appreciation of
end organ sensitivity (with respect to contraceptive steroids). Ralph Heywood, Chapter 7: Clinical Toxicity- could it
have been predicted? Post-marketing experience, Animal Toxicity Studies:
Their Relevance for Man (publ. Quay).

Risk
assessment policy that relies solely on screening bio-assay results from the
most sensitive species is not based on scientific principles. Neither is it
credible or reliable. Dr Vernon Houk, director
of environmental health at the American Center for Diseases Control, addressing
a conference in the USA, 1989, and quoted in Business Review Weekly, 27th April.

The principal
method of determining potential carcinogenicity of substances is based on
studies of daily administration of huge doses of chemicals to inbred rodents
for a lifetime. Then by questionable models, which include large safety
factors, the results are extrapolated to effects of minuscule doses in
humans... The rodent MTD test that labels plant chemicals as cancer-causing in
humans is misleading. The test is likewise of limited value for synthetic
chemicals. The standard carcinogen tests that use rodents are an obsolescent
relic of the ignorance of past decades. Philip H
Abelson, Science, vol 249, p 1357.

... numerous
chemicals have been found to have potential toxicity/carcinogenicity in rat or
mouse, which, we are reasonably certain, have little or no potential hazard in
man. The reason for this is again species differences, for the biological
defence mechanism which protects against toxic chemicals is most highly evolved
in man, who therefore generally has a higher resistance to chemical toxicity
and carcinogenicity than have rodents and other species… Parke, Ioannides and Lewis, Alternatives To
Laboratory Animals, vol 18, p 91-102.

1989

Elsewhere, I
have pointed out that overfeeding of rats profoundly influences the incidence
particularly of endocrine tumours. Furthermore, endocrine tumours and tumours
of tissues, such as the breast and uterus, which are very directly under
sex-hormone control, constitute a very high proportion of the tumours observed
in most carcinogenicity studies in rats. [Comparing] the incidences of tumours
in these categories in men and women with those in male and female rats...
[shows] the differences between the two species are sufficiently striking to
make one wonder how appropriate the laboratory rat is as a model for man in
terms of the spectra of tumours to which they are prone. Dr Francis Roe, Advances in Applied Toxicology, p 10, ed. A D Dayan & A J Paine (publ. Taylor
& Francis).

1988

There are
marked differences in carcinogenicity across sexes, strains and species. Often,
the-same chemical will cause one kind of cancer in one experiment and another
kind in another experiment Indeed, the most hard-bitten advocates of animal
experiments do not claim to be able to predict which organ will be affected in
humans by a chemical that is carcinogenic in animals. Freedman and Zeisel, Statistical Science, vol 3, p 3-28.

[Regarding
animal carcinogenicity tests on saccharin] Published risk estimates, starting
from the same animal data but using various [statistical] models, differ by
factors of over 5,000,000. Freedman and Zeisel, Statistical
Science, vol 3, p 3-28.

[Regarding
the difficulties of applying animal results to humans] "There turn out to
be many different ways to measure this difference [in size]. For example, a man
weighs 2800 times as much as a mouse, eats 300 times as much per day and lives
40 times as long. Which factor should be used to rescale the dose? Freedman and Zeisel, Statistical Science, vol 3, p 3-28.

There are many
unresolved problems in the standard bio-assay, including... how to account for
inter-species and intra-species differences in metabolism and pharmacokinetics. Omenn & Lave, Mutation Research, vol 205, p 41.

Data from
dose-response relationships are sometimes employed to estimate the expected
tumour incidence at dose levels very much lower than those which could possibly
be employed in conventional [animal] experiments. A number of mathematical
models have been employed in such estimates and the results obtained vary
considerably. Despite these uncertainties - and the possibly greater ones in
extrapolating from animals to man - such models are often employed in some
quarters to estimate the likely risk to man. Dr
Paul Grasso, Perspectives in Basic and Applied Toxicology, p268-284, ed. Ballantyne (publ. Butterworth).

Extrapolating
from one species to another is fraught with uncertainty... For almost all of-
the chemicals tested to date, rodent bio-assays have not been cost-effective.
They give limited and uncertain information on carcinogenicity, generally give
no indication of mechanism of action, and require years to complete."
[They are] "rarely the best approach for deciding whether to classify a
chemical as a human carcinogen. Lave, Ennever,
Rosenkrantz and Omenn, Nature, vol
336, p 631.

The standard
carcinogenicity bioassay, which involves treating two rodent species for a
minimum of 2 years, at a range of doses, is acknowledged to be an insensitive
tool because of the background `noise' of spontaneous disease. Most strains of
rat used in such studies have high incidence of pituitary and mammary tumours;
some inbred rat strains frequently develop leukaemia or testicular tumours;
mice strains show high incidence of malignant lymphomas and liver tumours. Dr Mary Tucker, Human Toxicology, vol 6, p107-109.

1986

If we wish to
understand human cancer, the [research] effort should be made in humans because
the genetic control seems to be different in different species. Renato Dulbecco (Nobel Laureate). Science, 231: 1055-1056.

Let us look at
some animal carcinogens – gold, DDT, clofibrate and bromocriptine. There
is no doubt that all of these can rightly be regarded as carcinogenic for
rodents, and yet there is really quite good evidence that they are not
carcinogenic to man. Prof Andre McLean, Long
Term Animal Studies-Their Predictive Value for Man (publ. MTP Press).

1985

During a
chronic study the problem may be complicated by the presence of concomitant
diseases; it is in fact known that acute inflammation or the presence of a
tumor may affect the kinetics of chemical, thus altering their potential
toxicity. Silvio Garattini, Toxic Effects of
Chemicals: Difficulties in extrapolating data from animals to man; Critical
Reviews in Toxicology, vol 16, issue
1, p1-29.

1984

It is
painfully clear that carcinogenesis in the mouse cannot now be predicted from
positive data obtained from the rat and vice versa. Dr F J Di Carlo, Drug Metabolism Reviews, vol 15, p 409-413.

1983

The major
problems of animal studies are the validity of cross-species comparisons and
relevance to human disease. Johanna Dwyer, Fundamental
& Applied Toxicology 3: 63-67.

The lifetime
feeding study of mice and rats appears to have less than a 50% probability of
finding known human carcinogens. On the basis of probability theory, we would
have been better off to toss a coin...The `definitive bioassay for
carcinogenesis' as now designed has never been subjected to proper validation
as an assay for human carcinogens. At attempt made in this paper to examine the
literature suggests that it may have an unacceptably high false negative rate
and that it produces so many contradictory answers as to suggest a very poor
specificity. Dr. David Salsburg, Fundamental
and Applied Toxicology, vol, 3, pp.
63-67.

1982

Animal model
systems in cancer research have been a total failure…not a single essential
drug for the treatment of human cancer was first picked up by an animal model
system. All of the drugs in wide current clinical use were only put into animal
model systems after finding clinical clues to their therapeutic possibility.
The money was spent…for two main reasons. First, it was a highly profitable
undertaking for certain medical schools and research institutions that were
incapable of doing any genuine cancer research. Second, it was sustained by a
superstitious belief in a grossly unscientific notion: mice are miniature
men…in sum, from the standpoint of current scientific theory of cancer, the
whole mystique of the animal model systems is hardly more than superstitious
nonsense…the moral is that animal model systems not only kill animals, they
also kill humans. There is no good factual evidence to show the use of animals
in cancer research has led to the prevention or cure of a single human cancer. Dr Irwin Bross, Dr Irwin Bross (formerly Director of
the Roswell Park Memorial Institute for Cancer Research) November issue, Fundamental
and Applied Toxicology.

The discovery
of chemotherapeutic agents for the treatment of human cancer is widely heralded
as a triumph due to the use of animal models… However, there is little, if any,
factual evidence that would support these claims… Indeed, while conflicting
animal results have often delayed and hampered advances in the war on cancer,
they have never produced a single substantial advance in either the prevention
or treatment of human cancer. Dr Irwin Bross
(formerly Director of the Roswell Park Memorial Institute for Cancer Research)
testifying to US Congress.

1980

Even when there
are common target sites for a given carcinogen, there are usually important
differences, between man and animals, and between different species and strains
of animals. These 'spontaneous' tumours in rats and mice... [vary] widely
according to sex, strain, diet, conditions of maintenance, hormonal status,
immunological status and latent virus infections. Dr
R L Carter, British Journal of Cancer,
vol 41, p 494.

…one of the
great fallacies in this calculation is that they are assuming that the mouse or
rat or the hamster predicts for man, and we have no basis for this
prediction…So it’s again a half-baked guess… Does the animal model have any
relevance to human disease? If not we’re wasting a lot of time, a lot of money,
a lot of good scientists, and a lot of good space at NIH… I completely agree
with Dr. Clayton that extrapolation is unscientific… the chief objective here
is to keep us all employed and to make sure we do interesting experiments so we
can keep coming back to nice places like this. Coulston
and Shubick (Eds) Human Epidemiology and Animal Laboratory Correlations in
Chemical Carcinogenesis, p391-3 and
p309 (publ. Ablex).

It is in fact
hard to find a single, common solid neoplasm [cancer] where management and
expectation of cure has been markedly affected by animal research. Most human
cancers differ from the artificially produced animal model… Harrison, Clinical Oncology, 15: 1-2.

We have a
discrepancy between animal data and human data…clearly, right now our animal
models are totally and absolutely inadequate to answer all the obvious
questions before us. Human
Epidemiology and Animal Laboratory Correlations in Chemical Carcinogenesis, Coulston and Shubick (Eds), p13 (Ablex Publ.).

1979

As a cancer
specialist engaged in clinical practice, I can’t agree with the researchers who
believe that results obtained with laboratory animals are applicable to human
beings. Dr Heinz Oeser, Quick, 15th March.

1976

Unfortunately,
extrapolations from animal results to man remains largely problematic and no
amount of mathematical sophistication can render such extrapolation more
certain. Higginson and Muir, Cancer Detection
and Prevention, 1(1) p79-105.

1952

Warning is
given not to carry over, without reservation, to man, the conclusions based on
animal experiments. In monkeys none of the powerful carcinogens [of man] has
been shown to produce cancers. The Lancet (1952) Aug 9, p 274.

1950

The
characteristic effects in leukaemia were detected solely as a result of
clinical observation. The various leukaemias in the mouse and rat were
relatively refractory to the influence of urethane, and the remarkable
effect in the human might have eluded discovery if attention had been
directed to the animal alone. That illustrates the hazards of such work. Dr Alexander Haddow, British Medical Journal, Dec 2, p1272.